Article date: October 1994
By: Eric Thorin, Christine Capdeville‐Atkinson, Bruno Corman, Jeffrey Atkinson, in Volume 113, Issue 2, pages 363-368
Age‐related changes in noradrenergic neurotransmission in the tail arteries of three rat strains: outbred Wistar (WI/Ico), inbred Wistar (WAG/Rij) and inbred Fischer (F344) have been compared in the present study.
The arterial noradrenaline content varied from 5 to 10 ng mg‐1 wet weight amongst young (3 to 6‐month old) representatives of each strain, but did not change with age. As protein content increased in senescent rats (24‐month old) by 30–40%, arterial tissue growth would not appear to receive a concomitant increase in sympathetic growth leading to relative, age‐related, structural sympathectomy in all strains.
The vasoconstrictor response to transmural electrical stimulation was diminished in adult and senescent rats of all strains.
As far as could be judged from the increase in noradrenaline release following perfusion with the α‐adrenoceptor antagonist, phentolamine (1 μm), the presynaptic α2‐adrenoceptor‐mediated inhibition of noradrenaline release was intact in old representatives of all strains.
With blockade of the two main systems which control noradrenaline release in the rat tail artery, viz, neuronal reuptake with cocaine (4 μm) and presynaptic α2‐adrenoceptors with phentolamine (1 μA), stimulation‐evoked release of noradrenaline was similar at all ages and in all strains. This suggests that in the rat tail artery the basic mechanism of neuronal release of noradrenaline is not functionally modified by aging.
We conclude that as sympathetic nerve terminals are apparently intact in all three strains of senescent rats used, the age‐associated deficit of α‐adrenergic control of vascular function is postsynaptic in nature.
Age‐related changes in noradrenergic neurotransmission in the tail arteries of three rat strains: outbred Wistar (WI/Ico), inbred Wistar (WAG/Rij) and inbred Fischer (F344) have been compared in the present study.
The arterial noradrenaline content varied from 5 to 10 ng mg‐1 wet weight amongst young (3 to 6‐month old) representatives of each strain, but did not change with age. As protein content increased in senescent rats (24‐month old) by 30–40%, arterial tissue growth would not appear to receive a concomitant increase in sympathetic growth leading to relative, age‐related, structural sympathectomy in all strains.
The vasoconstrictor response to transmural electrical stimulation was diminished in adult and senescent rats of all strains.
As far as could be judged from the increase in noradrenaline release following perfusion with the α‐adrenoceptor antagonist, phentolamine (1 μm), the presynaptic α2‐adrenoceptor‐mediated inhibition of noradrenaline release was intact in old representatives of all strains.
With blockade of the two main systems which control noradrenaline release in the rat tail artery, viz, neuronal reuptake with cocaine (4 μm) and presynaptic α2‐adrenoceptors with phentolamine (1 μA), stimulation‐evoked release of noradrenaline was similar at all ages and in all strains. This suggests that in the rat tail artery the basic mechanism of neuronal release of noradrenaline is not functionally modified by aging.
We conclude that as sympathetic nerve terminals are apparently intact in all three strains of senescent rats used, the age‐associated deficit of α‐adrenergic control of vascular function is postsynaptic in nature.
DOI: 10.1111/j.1476-5381.1994.tb16996.x
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